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Brain Hypoxia Secondary to Diffusion Limitation in Hypoxic Ischemic Brain Injury Postcardiac Arrest

Sekhon, Mypinder S. MD1; Ainslie, Philip N. PhD2; Menon, David K. MD, PhD3; Thiara, Sharanjit S. MD1; Cardim, Danilo PhD4; Gupta, Arun K. MBBS, PhD3; Hoiland, Ryan Leo PhD2; Gooderham, Peter MD5; Griesdale, Donald E. MD, MPH1,,4,,6

doi: 10.1097/CCM.0000000000004138
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Objectives: We sought to characterize 1) the difference in the diffusion gradient of cellular oxygen delivery and 2) the presence of diffusion limitation physiology in hypoxic-ischemic brain injury patients with brain hypoxia, as defined by parenchymal brain tissue oxygen tension less than 20 mm Hg versus normoxia (brain tissue oxygen tension > 20 mm Hg).

Design: Post hoc subanalysis of a prospective study in hypoxic-ischemic brain injury patients dichotomized into those with brain hypoxia versus normoxia.

Setting: Quaternary ICU.

Patients: Fourteen adult hypoxic-ischemic brain injury patients after cardiac arrest.

Interventions: Patients underwent monitoring with brain oxygen tension, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and jugular venous bulb oxygen saturation. Data were recorded in real time at 300Hz into the ICM+ monitoring software (Cambridge University Enterprises, Cambridge, United Kingdom). Simultaneous arterial and jugular venous bulb blood gas samples were recorded prospectively.

Measurements and Main Results: Both the normoxia and hypoxia groups consisted of seven patients. In the normoxia group, the mean brain tissue oxygen tension, jugular venous bulb oxygen tension, and cerebral perfusion pressure were 29 mm Hg (SD, 9), 45 mm Hg (SD, 9), and 80 mm Hg (SD, 7), respectively. In the hypoxia group, the mean brain tissue oxygen tension, jugular venous bulb oxygen to brain tissue oxygen tension gradient, and cerebral perfusion pressure were 14 mm Hg (SD, 4), 53 mm Hg (SD, 8), and 72 mm Hg (SD, 6), respectively. There were significant differences in the jugular venous bulb oxygen tension–brain oxygen tension gradient (16 mm Hg [sd, 6] vs 39 mm Hg SD, 11]; p < 0.001) and in the relationship of jugular venous bulb oxygen tension–brain oxygen tension gradient to cerebral perfusion pressure (p = 0.004) when comparing normoxia to hypoxia. Each 1 mm Hg increase in cerebral perfusion pressure led to a decrease in the jugular venous bulb oxygen tension–brain oxygen tension gradient by 0.36 mm Hg (95% CI, –0.54 to 0.18; p < 0.001) in the normoxia group, but no such relation was demonstrable in the hypoxia group.

Conclusions: In hypoxic-ischemic brain injury patients with brain hypoxia, there is an elevation in the jugular venous bulb oxygen tension–brain oxygen tension gradient, which is not modulated by changes in cerebral perfusion pressure.

1Division of Critical Care Medicine, Department of Medicine, Vancouver General Hospital, University of British Columbia, Vancouver, BC, Canada.

2Department of Health and Exercise Sciences, University of British Columbia – Okanagan, Kelowna, BC, Canada.

3Department of Clinical Neurosciences, Addenbrookes Hospital, University of Cambridge, Cambridge, United Kingdom.

4Department of Anaesthesiology, Pharmacology and Therapeutics, Vancouver General Hospital, University of British Columbia, Vancouver, BC, Canada.

5Division of Neurosurgery, Department of Surgery, Vancouver General Hospital, University of British Columbia, Vancouver, BC, Canada.

6Centre for Clinical Epidemiology and Evaluation, Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, BC, Canada.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (http://journals.lww.com/ccmjournal).

Supported, in part, by grant from the Laerdal Foundation.

Dr. Sekhon’s institution received funding from Laerdal Foundation; he received funding from the Clinician Scientist Award from Vancouver Coastal Health Research Institute. Dr. Menon received support for article research from National Institute for Health Research, United Kingdom. Dr. Gooderham received funding from consulting for Stryker Canada and Baxter Canada, and research grants from Brain Aneurysm Foundation and Rare Diseases Foundation (research into Moyamoya disease). Dr. Griesdale is funded through a Health-Professional Investigator Award from the Michael Smith Foundation for Health Research. The remaining authors have disclosed that they do not have any potential conflicts of interest.

Trial Registration: NCT03609333—ClinicalTrials.gov.

For information regarding this article, E-mail: mypindersekhon@gmail.com

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